Key result
Suspected snake envenomation triggers fatal anterior STEMI and refractory VT despite successful LAD stenting.
Why the study?
Snake envenomation is an uncommon but potentially catastrophic cause of cardiovascular toxicity—including direct myocardial ischemia, malignant arrhythmias, and cardiogenic shock—that is often underestimated and poses significant diagnostic and therapeutic challenges for cardiology teams.
Case Report (n=1)
No
This case report highlights that snake envenomation can trigger fatal thrombotic coronary occlusion, malignant arrhythmias, and refractory cardiogenic shock even after successful mechanical revascularization, underscoring the need for early recognition and prompt antivenom administration.
Answers are grounded in this paper and cite their sources.
Snake envenomation may cause fatal STEMI despite PCI; leaves open whether early antivenom prevents refractory shock.
Background: Snake envenomation is a globally recognized neglected tropical disease that remains uncommon but potentially a catastrophic cause of cardiovascular toxicity. It has been documented to have hemotoxic and neurotoxic effects, along with its ability to induce direct myocardial ischemia, malignant arrhythmias, and cardiogenic shock that is often underestimated, particularly in non-endemic regions. Venom components can trigger a "thrombotic storm" through direct endothelial injury and hypercoagulability, posing significant diagnostic and therapeutic challenges for cardiology teams. Case presentation: Our case describes a 72-year-old Moroccan man with no documented prior comorbidities who presented to the emergency department with a one-week history of progressive dyspnea, orthopnea, and palpitations, later confirmed to have an acute anterior ST-segment elevation myocardial infarction (STEMI). He was immediately referred to our center for lifesaving intervention. Coronary angiography revealed a total proximal left anterior descending (LAD) artery occlusion in the absence of diffuse atherosclerotic disease. Despite successful primary percutaneous coronary intervention (PCI) with restoration of Thrombolysis in Myocardial Infarction (TIMI) grade III flow, the patient developed recurrent ventricular tachycardia and refractory cardiogenic shock. A subsequent physical examination revealed a bleeding wound on the right shoulder with two distinct pinpoint puncture marks, raising a high clinical suspicion of snake envenomation. Despite aggressive resuscitation efforts and a consultation with the National Toxicology Center for antivenom administration, the patient suffered a final pulseless cardiac arrest and was pronounced dead. Conclusion: This case highlights a rare but lethal intersection between snake envenomation and the development of acute myocardial infarction. It highlights a paradox where dual antiplatelet therapy might be neutralized by venom-derived enzymes, leading to rapid clinical deterioration despite successful mechanical revascularization. These findings emphasize that envenomation must remain part of the differential diagnosis in cases of atypical STEMI. Early clinical recognition, multidisciplinary collaboration with toxicology experts, and the availability of anti-venom therapy even in regions where snake bites are uncommon are critical factors for improving survival.
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Alhazmi et al. (2026) conducted a case report in Acute anterior ST-segment elevation myocardial infarction following snake envenomation (n=1). Snake envenomation was evaluated on Survival / Clinical course. Suspected snake envenomation in a 72-year-old man caused acute anterior STEMI from proximal LAD occlusion, leading to LVEF of 10%, refractory ventricular tachycardia, and death despite TIMI III flow.
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